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目的探讨重组人表皮生长因子(rhEGF)联合前列地尔对糖尿病溃疡Wnt/β-连环素(β-Catenin)信号通路的作用。方法糖尿病皮肤溃疡大鼠模型随机分为4组。对照组注射用生理盐水冲洗创面;rhEGF组rhEGF凝胶涂抹创面;前列地尔组尾静脉推注前列地尔;联合给药组同时予rhEGF和注射用前列地尔治疗。观察各组皮肤愈合情况,治疗后第14天测溃疡创面Wnt-1、β-Catenin、糖原合成酶激酶-3(GSK-3β)mRNA和蛋白的表达。结果给药后第6、10和14天时联合给药组溃疡面愈合率为(9.76±2.37)%、(35.74±3.65)%、(51.37±4.16)%及(84.42±5.35)%,均较rhEGF组和前列地尔组增加(P<0.05);给药后14d时联合给药组溃疡面Wnt-1、β-Catenin和GSK-3βmRNA表达分别为(1.42±0.19)、(1.56±0.21)和(0.95±0.15),均较rhEGF组和前列地尔组增加(P<0.05);给药后14d时联合给药组溃疡面Wnt-1、β-Catenin和GSK-3β蛋白的表达分别为(1.17±0.16)、(1.38±0.18)和(0.81±0.13),均较rhEGF组和前列地尔组增加(P<0.05)。结论 rhEGF联合前列地尔可促进糖尿病溃疡的愈合,并通过上调Wnt-1、β-Catenin和GSK-3β的表达而起到调节Wnt/β-Catenin信号通路的功能。
Objective To investigate the effect of recombinant human epidermal growth factor (rhEGF) and alprostadil on the Wnt / β-catenin signaling pathway in diabetic ulcer. Methods Diabetic skin ulcer rats were randomly divided into 4 groups. In the control group, the wounds were rinsed with saline; the rhEGF gel was applied to the wounds in the rhEGF group; the alprostadil was injected into the tail vein of the alprostadil group; and the rhEGF and the prostaglandin for injection were administered simultaneously in the combination group. The wound healing of each group was observed. The expression of Wnt-1, β-Catenin and glycogen synthase kinase-3 (GSK-3β) mRNA and protein were detected on the 14th day after treatment. Results The rates of ulcer healing in the combination group were (9.76 ± 2.37)%, (35.74 ± 3.65)%, (51.37 ± 4.16)% and (84.42 ± 5.35)% on the 6th, The expressions of Wnt-1, β-Catenin and GSK-3βmRNA in the ulcer group were (1.42 ± 0.19) and (1.56 ± 0.21) days, respectively, at the 14th day after the administration of rhEGF and alprostadil (P <0.05) And (0.95 ± 0.15), respectively, compared with those in rhEGF group and alprostadil group (P <0.05). The expressions of Wnt-1, β-Catenin and GSK-3β in ulcer- (1.17 ± 0.16), (1.38 ± 0.18) and (0.81 ± 0.13), respectively, compared with rhEGF group and alprostadil group (P <0.05). Conclusion rhEGF combined with alprostadil can promote the healing of diabetic ulcer, and regulate the function of Wnt / β-Catenin signaling pathway by up-regulating the expression of Wnt-1, β-Catenin and GSK-3β.